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Am J Physiol Regul Integr Comp Physiol 281: R987-R993, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 3, R987-R993, September 2001

Role of the renin-angiotensin system during alterations of sodium intake in conscious mice

Brian C. Cholewa and David L. Mattson

Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

The present studies were performed to quantify circulating components of the renin-angiotensin-aldosterone axis and to determine the functional importance of this system during alterations in sodium intake in conscious mice. Increasing sodium intake from ~200 to 1,000 µeq/day significantly decreased plasma renin concentration from 472 ± 96 to 304 ± 83 ng ANG I · ml-1 · h-1 (n = 5) but did not alter plasma renin activity from the low-sodium level of 7.7 ± 1.1 ng ANG I · ml-1 · h-1. Despite the elevated plasma renin concentration, plasma ANG II in mice on low-sodium level averaged 14 ± 3 pg/ml and was significantly suppressed to 6 ± 1 pg/ml by high-sodium intake (n = 7). Consistent with the modulation of ANG II, plasma aldosterone significantly decreased from 41 ± 8 to 8 ± 3 ng/dl when sodium intake was elevated (n = 6). In a final set of experiments, the continuous infusion of ANG II (20 ng · kg-1 · min-1) led to a mild salt-sensitive increase in mean arterial pressure from 108 ± 2 to 131 ± 2 mmHg as sodium intake was varied from low to high (n = 7). In vehicle-infused mice, mean arterial pressure was unaltered from 109 ± 2 mmHg when sodium intake was increased (n = 6). These studies indicate that the physiological suppression of circulating ANG II may be required to maintain a constancy of arterial pressure during alterations in sodium intake in normal mice.

aldosterone; blood pressure


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